In healthy people, hypoxia results in a marked accentuation of breathing. If the oxygen content in the blood falls below a critical value, serious effects occur with persistent hypoxia, for example metabolic derangement owing to production of lactic acid, tissue acidosis, cell damage. The brain and heart are at particular risk. The possible consequences of cerebral impairment are neuromuscular coordination disorders, a diminution in judgment, visual disturbances, sweats, collapse and unconsciousness, increase in cerebral pressure, convulsions and loss of brain tissue. The cardiac disorders which could result are, for example, ventricular extrasystoles, ventricular fibrillation, cor pulmonale (right ventricular strain) and changes in the walls of pulmonary vessels.
Hypoxic states are frequently the consequence of breathing difficulties. A deficiency of respiratory drive owing to impairment of the regulatory systems in the central nervous system is often evident only under resting conditions. Thus, as is known, breathing difficulties in premature babies resulting from immature brain structures, and breathing difficulties in early childhood may cause what is called sudden infant death syndrome (SIDS) in the first few months of life. The hazard in this context is prolonged and often unrecognized hypoxic states during sleep, with a pathological lack of an accentuation of breathing, so that damage in the central and autonomic nervous systems and in the cardiopulmonary system can arise.
The use of ventilation equipment for the temporary treatment of breathing difficulties is known. Also known is the electrical stimulation of phrenic nerves for artificial initiation of breathing movements. Likewise known is the pharmacological treatment of difficulties of this type. In the context of therapy of breathing difficulties in premature babies, oxygen therapy, for example, an oxygen tent, has frequently been used. However, the known oxygen therapy of premature babies may result in blinding and damage to the lungs with impairment of gas exchange.
Where patients with central breathing difficulties are artificially ventilated using ventilating equipment, although the gas exchange, which is absolutely necessary for life is maintained, the therapeutic measures for restoring spontaneous breathing are inadequate. It is known that when prolonged artificial ventilation is used, patients may lose, at least temporarily, the ability to breathe spontaneously.
It has been found that electrical stimulation of the phrenic nerves could cause irreversible damage to the nerves, and, frequently, uncoordinated breathing movements, so that a tracheotomy is necessary to avert airway blockage.
Pharmacological therapy is often unsuccessful or only temporarily successful, and it may result in drug dependence and may have drastic adverse effects on sleeping behavior.
The known treatment methods described herein frequently have the disadvantage that the patient loses the ability to breathe spontaneously because the breathing reflexes are not trained. Nor is there promotion of maturation of the respiratory system which in premature babies is frequently insufficiently advanced.
Given the lack of suitable therapeutic approaches, to date people have been confined to using apnoea monitors, in particular as equipment in the homes of babies at risk from sudden infant death syndrome (SIDS). When breathing is interrupted, the monitor generates a visible or audible alarm which wakes the sleeper. It is disadvantageous that, with this action which is exclusively for rescue, there is neither elimination of the danger of chronic hypoxia nor support for the maturation of the breathing reflex.
Because of the dangers and side effects of the current therapeutic options which have been discussed, as a rule only serious breathing difficulties are treated. On the other hand, untreated breathing difficulties can result in fatal disorders, for example, SIDS.